Other factors associated with OA hand pain include structural and inflammatory changes and demographic/psychosocial parameters, reported the researchers, led by Karin Magnusson, MSc, national advisory unit on rehabilitation in rheumatology at Diakonhjemmet Hospital in Oslo. Furthermore, the determinants of pain appear to differ depending on disease phenotype -- erosive or non-erosive.

"Currently no disease-modifying drugs exist for OA. However, more nuanced knowledge about hand OA pain may be relevant for future targeted pain prevention and management," wrote Magnusson and colleagues.

Given the limited knowledge about the drivers of pain and disability in hand OA, the study aimed to explore a broad range of potential explanatory factors, particularly different determinants in the two disease subgroups. The investigation formed part of the Musculoskeletal Pain in Ullensaker Study, a cross-sectional population-based analysis of 12,155 people with questionnaire-reported OA.

Of 1,049 eligible respondents with self-reported OA, 630 underwent clinical examination at Diakonhjemmet Hospital with radiography and ultrasonography of the hips, knees, and hands as well as assessment by American College of Rheumatology criteria. Of these, 530 had radiographic hand OA (>1 hand joint with Kellgren-Lawrence grade >2) and were eligible to participate in the study, which excluded those with inflammatory joint disease. Their mean age was 65 (40 to 79) and 71% were women.

Comorbidities such as hypertension, diabetes mellitus, widespread pain and mental health were also recorded, as was treatment with various analgesics and anti-inflammatories.

The 131 patients diagnosed with erosive hand OA tended to be older and female and to have more severe radiographic changes, more synovitis, and more frequent combined finger and thumb OA than those with non-erosive disease. The median number of erosions was 3 (interquartile range 1.0-5.6).

Median AUSCAN pain was significantly higher in participants with both OA and diabetes mellitus than for those with erosive OA but without diabetes: 9 (IQR 7-11) versus 5 (IQR 1-9, P=0.004).

Inflammatory and structural OA features such as synovitis were associated with pain only in erosive hand OA, whereas joint characteristics were of little or no relevance in non-erosive OA, in which only factors outside the joints explained pain variance.

The researchers reported a negative association between hypertension and hand pain, and a significant association with infrequent alcohol consumption emerged only in non-erosive OA.

The present study, the authors said, is the first to show that diabetes is associated with pain in erosive hand OA independently of BMI. Previous studies have noted a higher frequency of obesity, as well as of hypertension, dyslipidemia, and metabolic syndrome.

"Our study forms a basis for future prospective cohort studies and intervention studies, which might show that intervening in diabetes may reduce hand OA risk or decrease the severity of hand pain," Magnusson told MedPage Today.

The reasons behind the diabetes-hand pain connection are unclear. "Poorly regulated diabetes mellitus is a risk factor for developing neuropathy, which may lead to increased pain," the authors speculated. Diabetes may also cause low-grade systemic inflammation resulting in more pain, a hypothesis supported by the observed association between diabetes and a higher number of joints with synovitis.

As for the study's immediate clinical implications, Magnusson said, "I think we should study the association between diabetes and hand OA further before recommending that OA patients with accelerating hand pain be tested for diabetes."

Addressing the limitations of the study, the Oslo researchers noted that its cross-sectional design made it difficult to draw conclusions about causality. And the relatively small number of participants with erosive hand OA (124 for whom data was complete) may have resulted in less robust estimates in the structural equation analyses. In addition, under physical activity, there was no information collected specifically on hand activity, nor was there any data on features imaged by MRI, the only means of visualizing the bone marrow lesions associated with joint tenderness in hand OA. Furthermore, participants' self-reporting of diabetes may have risked misclassification of those who were not actually treated for diabetes.

The investigators called for longitudinal studies to further evaluate the role of diabetes mellitus in OA pathogenesis as well as its association with pain in (erosive) hand OA.

This study was supported by the South-Eastern Norway Regional Health Authority.

One of the authors reported receiving honoraria and consulting or speaking fees from several pharmaceutical companies.

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